AB0624 DUAL TRAJECTORIES OF DSDNA AND C3 CORRELATED WITH MORTALITY IN SYSTEMIC LUPUS ERYTHEMATOSUS
Authors: H. H. Chen, W. N. Huang, T. Y. Hsieh, Y. H. Chen
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by diverse clinical manifestations with multi-organ damage and an increased risk of mortality. Several clinical characteristics have been identified as predictors of overall mortality in patietns with SLE, including oragan damage, time from onset to diagnosis &gt; 1 year, nephropathy, male gender, older age of onset, high Systemic Lupus Eythematosus Disease Activity Index (SLEDAI) scores and high Age-adjusted Charlson Comorbidity Index (ACCI) scores. However, whether trajectories of dsDNA and C3, two of the frequently monitored immune profiles, are associated with mortality among patients with SLE is still unknow. We aimed to assess the association of mortality with dual trajectories of dsDNA and C3 within two years in a large Taiwanese lupus cohort. <h3>Objectives</h3> We aimed to assess the association of mortality with dual trajectories of dsDNA and C3 within two years in a large Taiwanese lupus cohort. <h3>Methods</h3> The study linked electronic medical record data at Taichung Veterans Genral hospital to the file of Cause of Death Data from the National Health Insurance Research Database managed by Center for Helath and Welfare Data Science in Taiwan. From Jan 1, 2000 to Mar 31, 2021, we identified 4850 patients with SLE who were followed up at TCVGH. We excluded 131 patients who were dead and 364 patients who were lost to follow-up withing 2 years. We also excluded 1999 patients who did not have at less 2 records of paired dsDNA and C3 data ever 3 months during the first two-years. We finally included 2,356 patients for trajectories analysis. The first 2 years of follow-up was used to establish trajectories of dsDNA and C3. We calculated the man ± standard deviation of dsDNA and C3 for the eight 3-month intervals and we used these data separately for trajectory determination, which was by group-based trajectory analysis with a latent class growth model, fitting the SAS Proc Traj procedure. We classified patients with SLE into 4 groups (G) based on dual trajectories of dsDNA and C3: G1- lowest dsDNA and second highest C3 trajectory (41.6%); G2- lowest dsDNA and highest C3 trajectory (32.0%); G3- second highest dsDNA and second highest C3 trajectory (19.2%); group 4, highest dsDNA and lowest C3 trajectory (7.1%). The relative risk of mortality was estimated using Cox proportional hazard model adjusting for age, gender, hypertension, diabetes mellitus and hyperlipidemia, shown as hazard ratios (HRs) with 95% confidence intervals (CIs). <h3>Results</h3> The proportions of female in G1-G4 were 88.0%, 87.0%, 86.7% and 84.0% respectively. The mean age in G1-G4 were 37.6 years, 41.3 years, 36.4 years and 34.7 years respectively. The mortality rates were highest in G1 (6.24 cases per 1,000 person-years), followed by G2 (5.90 cases per 1,000 person-years), G3 (5.04 cases per 1,000 person-years) and G4 (4.19 cases per 1,000 person-years). After adjusting for potential confounders, the risk of mortality in G1 was significantly higher in G2 (HR, 1.67; 95% CI, 1.10–2.53; p = 0.016), but not in G3 (HR, 1.16; 95% CI, 0.66–2.05; p = 0.605) and G4 (HR, 1.22; 95% CI, 0.51–2.91; p = 0.659) as compared to that in G2. Other significant independent predictors of mortality included age (HR, 1.05; 95% CI, 1.04–1.06; p &lt; 0.001) and hypertension (HR, 1.83; 95% CI, 1.14–2.95; p = 0.013). <h3>Conclusion</h3> This single center study revealed that SLE patients with lowest dsDNA and second highest C3 trajectory had a significantly higher risk of mortality than SLE patients with lowest dsDNA and highest C3 trajectory. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.